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排序方式: 共有1687条查询结果,搜索用时 15 毫秒
1.
目的研究黄芩苷通过iNOS/PUMA信号通路促进肝星状细胞凋亡的作用。方法MTT检测细胞增殖抑制率,Western Blot检测iNOS、PUMA蛋白表达,real-time PCR检测PUMA mRNA表达,一氧化氮检测试剂盒检测NO含量,iNOS抑制剂L-NAME预处理后检测细胞增殖抑制率和PUMA表达,Hoechst 33342核染色检测细胞凋亡。结果50 mM黄芩苷引起肝星状细胞活化诱导性死亡;黄芩苷促进肝星状细胞PUMA mRNA、蛋白表达;iNOS抑制剂L-NAME预处理后PUMA表达降低、细胞凋亡减少。结论黄芩苷能通过iNOS/PUMA信号通路促进肝星状细胞凋亡。  相似文献   
2.
目的 探讨小剂量超短波对脊髓损伤患者功能恢复效果及对血清诱导型一氧化氮合酶(iNOS)、肿瘤坏死因子-α(TNF-α)、血管内皮生长因子(VEGF)、脑源性神经营养因子(BDNF)表达的影响。 方法 收集60例脊髓损伤患者,随机分为治疗组与对照组,每组30例。对照组给予基础康复治疗,治疗组加用小剂量超短波治疗,共治疗3个疗程。评估疗效并分析影响脊髓功能恢复的因素。 结果 治疗组总有效率高于对照组(P<0.05);康复治疗后,治疗组ASIA量表运动功能、感觉功能评分高于对照组(P<0.05);血清VEGF、BDNF表达含量高于对照组(P<0.05),iNOS、TNF-α表达含量低于对照组(P<0.05);小剂量超短波治疗是脊髓损伤患者预后的保护因素(P<0.05)。 结论 小剂量超短波辅助治疗可明显促进患者脊髓功能恢复,其机制可能与下调血清iNOS、TNF-α表达,上调VEGF、BDNF表达有关。  相似文献   
3.
This study was carried out to evaluate the protective effects of Panax ginseng aqueous extract (GAE) against hepatorenal toxicity induced by lambda‐cyhalothrin‐acetamiprid insecticide mixture in rats. A total of 32 male albino rats were assigned into four groups. Normal control group received distilled water. Insecticide control group intoxicated with the insecticide at a dose of 2.14 mg/kg b.wt orally day after day for 45 days. GAE control group was treated with GAE at a dose 200 mg/kg b.wt orally. GAE experimental group was administered GAE 1 hour before insecticide administration. Intoxication of rats with the insecticide caused a significant increase in serum aspartate aminotransferase and alanine aminotransferase activities and urea and creatinine levels as well as malondialdehyde concentration and proteins expression of caspase‐3 and induced nitric oxide synthase in hepatic and renal tissues. However, it decreased the serum levels of total protein and globulin and reduced the glutathione content and catalase activity in hepatic and renal tissues. In addition, insecticide induced histopathological alterations in both hepatic and renal tissues. In contrast, GAE modulated insecticide‐induced alterations in liver and kidney functions and structures as it ameliorated the effects of insecticide on the above mentioned parameters. These results indicated that GAE was a potent antioxidant agent that could protect rats against insecticide‐induced hepatorenal toxicity.  相似文献   
4.
目的探讨白藜芦醇(Res)对脓毒症血管舒张反应性的保护作用及与eNOS和iNOS的关系。方法采用盲肠结扎穿孔复制脓毒症模型,将32只SD大鼠随机分为4组:正常对照组、脓毒症组、常规治疗组(乳酸林格液体复苏+血管活性药多巴胺+头孢呋辛钠)、Res治疗组(Res+常规治疗),每组8只。Res治疗组在模型后尾静脉给予白藜芦醇,12 h后行常规复苏并二次给药,观察4组大鼠肠系膜上动脉(SMA)的舒张反应性、肠系膜微血管动静脉流速、血流动力学、肝肾血流量、肠系膜上动脉eNOS和iNOS的表达及存活率和存活时间的变化。结果与正常对照组相比,脓毒症组大鼠血管舒张反应性明显降低;常规复苏可轻微改善脓毒症大鼠血管舒张反应性;Res可以明显改善脓毒症大鼠肠系膜血管舒张反应性,进一步研究发现,Res通过保护脓毒症大鼠的血管舒张反应性来改善血流动力学和组织器官的灌注量,提高了脓毒症大鼠的存活率和存活时间,机制研究发现Res对脓毒症大鼠血管舒张反应性的保护作用与血管eNOS和iNOS有关。结论白藜芦醇通过改善脓毒症大鼠的血管舒张反应性,从而实现了对整体器官的保护作用。  相似文献   
5.
目的:研究诱导型一氧化氮合成酶(iNOS)、血管内皮生长因子(VEGF)在子宫内膜异位症(EMs)的异位内膜的表达.方法:采用免疫组织化学方法分别检测30例EMs异位内膜与35例正常对照组子宫内膜组织中iNOS、VEGF的表达,了解异位内膜组织中iNOS、VEGF表达的相关性.结果:在EMs的异位内膜组织中,iNOS和VEGF蛋白的表达明显高于正常子宫内膜组织的表达;在EMs异位子宫内膜组织中,iNOS和VEGF的表达成正相关(r=0.895,P<0.05).结论:EMs中,异位内膜组织的侵袭力增强及血管生成可能与iNOS、VEGF高表达有关.  相似文献   
6.
赵精咪  孙莉  梁浩  程焱 《天津医药》2019,47(3):235-240
目的 探索U0126对脑组织谷氨酸神经毒性的保护作用及可能机制。方法 健康成年雄性SD大鼠皮层注射 N-甲基-D-天冬氨酸(NMDA)建立脑组织谷氨酸神经毒性模型。首先,采用不同浓度 NMDA(50、100、200mmol/L)及处理不同时间(3、6、12、24 h)筛选最佳的建模条件。根据选定的最佳条件,实验设对照组、MAPK/ERK1/2抑制剂U0126单独处理组(2 g/L)、NMDA组(200 mmol/L)、不同浓度(0.5、1、2 g/L)U0126联合NMDA处理组。各组处理24 h后处死动物,脑组织切片后行HE染色组织评价损伤;蛋白质印迹法检测损伤部位环氧合酶-2(COX-2)、诱导型一氧化氮合酶(iNOS)、Caspase-3(活化形式)及磷酸化ERK1/2(p-ERK1/2)表达水平,确定U0126在脑组织谷氨酸神经毒性损伤中的保护作用。结果 (1)NMDA以时间和浓度依赖的方式导致大鼠皮层兴奋毒性损伤,激活MAPK/ERK1/2信号通路,加重脑组织损伤,选取200 mmol/L NMDA处理24 h进行建模。(2)与对照组相比,NMDA组脑损伤部位COX-2、iNOS、Caspase-3(活化形式)、p-ERK1/2表达明显增加。U0126+NMDA处理组与NMDA组相比,COX-2、NOS、Caspase-3(活化形式)、p-ERK1/2表达水平随U0126浓度升高而降低,脑损伤的面积显著减小。结论 U0126对大鼠皮层谷氨酸神经毒性损伤具有保护作用,其机制可能与抑制ERK1/2激活及其下游的炎症、凋亡信号途径有关。  相似文献   
7.
Microglial polarization to the anti-inflammatory M2 phenotype is essential in resolving neuroinflammation, making it a promising therapeutic strategy for stroke intervention. The actin cytoskeleton is known to be important for the physiological functions of microglia, including migration and phagocytosis. Profilin 1 (PFN1), an actin-binding protein, is involved in the dynamic transformation and reorganization of actin. However, the role of PFN1 in microglial polarization and ischemia/reperfusion injury is unclear. The role of PFN1 on microglial polarization was examined in vitro in BV2 microglial cells subjected to oxygen-glucose deprivation/reoxygenation (OGDR) and in vivo in male mice after transient middle cerebral artery occlusion (MCAO). Knockdown of PFN1 inhibited M1 microglial polarization and promoted M2 microglia polarization 48 hr after OGDR stimulation in BV2 cells and 7 days after MCAO-induced injury in male mice. RhoA/ROCK pathway was involved in the regulation of PFN1 during microglial polarization. Knockdown of PFN1 also significantly attenuated brain infarcts and edema, improved cerebral blood flow and neurological deficits in MCAO-injured mice. Inhibition of PFN1 effectively protected the brain against ischemia/reperfusion injuries by promoting M2 microglial polarization in vitro and in vivo.  相似文献   
8.
9.
The present study showed that silymarin, a polyphenolic flavonoid isolated from milk thistle (Silybum marianum), inhibited lipopolysaccharide (LPS)-induced morphological changes in the mouse RAW264.7 macrophage cell line. We also showed that silymarin inhibited the nuclear translocation and transactivation activities of nuclear factor-kappa B (NF-κB), which is important for macrophage activation-associated changes in cell morphology and gene expression of inflammatory cytokines. BAY-11-7085, an NF-κB inhibitor, abrogated LPS-induced morphological changes and NO production, similar to silymarin. Treatment of RAW264.7 cells with silymarin also inhibited LPS-stimulated activation of mitogen-activated protein kinases (MAPKs). Collectively, these experiments demonstrated that silymarin inhibited LPS-induced morphological changes in the RAW264.7 mouse macrophage cell line. Our findings indicated that the most likely mechanism underlying this biological effect involved inhibition of the MAPK pathway and NF-κB activity. Inhibition of these activities by silymarin is a potentially useful strategy for the treatment of inflammation because of the critical roles played by MAPK and NF-κB in mediating inflammatory responses in macrophages.  相似文献   
10.
Prior findings in vitro of a TGF-β3 dependent mechanism induced by low dose-rate irradiation and resulting in increased radioresistance and removal of low dose hyper-radiosensitivity (HRS) was tested in an in vivo model. DBA/2 mice were given whole-body irradiation for 1 h at low dose-rates (LDR) of 0.3 or 0.03 Gy/h. Serum was harvested and added to RPMI (4% mouse serum and 6% bovine serum).This medium was transferred to reporter cells (T-47D breast cancer cells or T98G glioblastoma cells). The response to subsequent challenge irradiation of the reporter cells was measured by the colony assay. While serum from unirradiated control mice had no effect on the radiosensitivity in the reporter cells, serum from mice given 0.3 Gy/h or 0.03 Gy/h for 1 h removed HRS and also increased survival in response to doses up to 5 Gy. The effect lasted for at least 15 months after irradiation. TGF-β3 neutralizer added to the medium containing mouse serum inhibited the effect. Serum from mice given irradiation of 0.3 Gy/h for 1 h and subsequently treated with iNOS inhibitor 1400W did not affect radiosensitivity in reporter cells; neither did serum from the unirradiated progeny of mice given 1h LDR whole-body irradiation.  相似文献   
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